Development of chronic bladder ischemia rat model for reproducing the detrusor underactivity

Non-Moderated Poster Session

12:30 PM - 1:30 PM

Dr. Jung Hyun Shin (1), Hwan Yeul Yu (1), Ji-Yeon Han (2), Dong-Myung Shin (3), Myung-Soo Choo (1)

(1) Department of Urology, Asan Medical Center, Seoul, South Korea, (2) Department of Urology, Pusan National University Yangsan Hospital, Yangsan, South Korea, (3) Department of Biomedical Sciences Asan Medical Center, Seoul, South Korea

To develop a rat model of chronic bladder ischemia and to investigate the effect of chronic bladder ischemia on voiding behavior and bladder function.

AIMS

Adult male rats were divided into four groups. The arterial injury (AI) group underwent endothelial injury of the iliac arteries (AI-10, 10 times of injury at each iliac artery; AI-20, 20 times; AI-30, 30 times) and received a 2% cholesterol diet. The sham group underwent sham operation and received a 2% cholesterol diet. The control group received a regular diet. After 8 weeks, a metabolic cage study and cystometry were performed without anesthesia. Histological examination of the iliac arteries and the bladder was performed. The bladder was also processed for organ bath study.

METHODS

The metabolic cage study showed that in the AI-30 group, micturition interval, voided volume, and Results: The metabolic cage study showed that in the AI-30 group, micturition interval, voided volume, and residual volume were significantly increased. Cystometry showed that the frequency of reflex bladder contractions and micturition pressure were significantly lower in the AI-30 group. Histological study showed that in the AI group alone, atherosclerotic occlusion occurred in the iliac arteries as well as in the downstream bladder microvessels. Contractile responses of bladder strips to various stimuli in AI-30 group were significantly less than in sham group.

RESULTS

Pelvic arterial occlusive disease plus vascular endothelial dysfunction may cause progressive vascular damage resulting in bladder dysfunction that develops the detrusor underactivity

CONCLUSIONS